Lithium-induced diabetes insipidus-like syndrome

Angrist, Burton; Gershon, Samuel; Levitan, Stephan J.; Blumberg, A

doi:10.1016/0010-440x(70)90155-0

Cited by 109 publications

(36 citation statements)

References 7 publications

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“…Unfortunately, important side effects have been reported in patients chronically treated with lithium (2-4). The most prominent was polyuria associated with polydipsia (5)(6)(7)(8)(9)(10) Receivedfor publication 11 July 1985. (ADH)' release (11)(12)(13). Nevertheless, the fully developed syndrome usually displays all the features of a nephrogenic type of diabetes insipidus (6,(9)(10)(11)(13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

Inhibition by lithium of the hydroosmotic action of vasopressin in the isolated perfused cortical collecting tubule of the rabbit.

Cogan¹,

Abramow²

1986

J. Clin. Invest.

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Because treatment with lithium salts may impair renal concentrating ability, we investigated the possibility of a direct effect of lithium ions on the permeability to water of the collecting duct epithelium. The coefficient of hydraulic conductivity (Lp) of isolated perfused rabbit cortical collecting tubules (CCT) was measured in the presence and absence of arginine-8-vasopressin (AVP), or 8-bromo (Br) cyclic AMP (cAMP) and/or lithium chloride (Li 10 mM). In the absence of AVP, Li in the lumen for 30 min failed to affect basal water permeability; however, in tubules preincubated with Li in the lumen for 80 min, basal water permeability was reduced to 30% of the value found in control tubules (P < 0.01). In CCT incubated at 25°C with Li in the lumen for 3 h, the hydroosmotic response to 2.5 sU -ml-E AVP (Lp = 6.88±1.54 nl cm-2. S-atm-n) was significantly lower than that in the control tubules (13.98±1.59, P < 0.01); the inhibition was not reversible. When Li was present in the peritubular medium only, the hydroosmotic effect of AVP was not different from that of the controls. The hydroosmotic effect of 25 uU/ml AVP was investigated at 37°C. CCI exposed to Li in the lumen had a 49% inhibition of peak Lp under AVP (Lp= 10.98±1.17) as compared with control tubules (L, = 21.39±1.51; P < 0.005). In contrast, the hydroosmotic response to 8-Br-cAMP was not affected by lithium. The results are compatible with the view that Li inhibits the action of AVP at the level of the regulating protein or the catalytic unit of the membrane adenylate cyclase and that the site of the interaction can be reached by lithium only from the cytoplasmic side. The Li-antidiuretic hormone (ADH) interaction found here may represent the earliest pathophysiological event underlying the renal concentrating defect observed after Li administration.

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Section: Introductionmentioning

confidence: 99%

Inhibition by lithium of the hydroosmotic action of vasopressin in the isolated perfused cortical collecting tubule of the rabbit.

Cogan¹,

Abramow²

1986

J. Clin. Invest.

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“…Goodwin & Jenner (1967) have presented evidence that at least in some recurrent psychoses there are large changes in the antidiuretic activity of the urine occurring simultaneously with the changing mental state. Angrist, Gershon, Levitan & Blumberg (1970) have reported the antidiuretic hormone resistance of the polyunria caused by lithium in some patients. Schou (1958) and Thomsen (1971) have shown that the polyuria more easily induced in rats by lithium is also resistant to the action of antidiuretic hormone.…”

Section: Introductionmentioning

confidence: 99%

Some aspects of the inhibition of the action of antidiuretic hormone by lithium ions in the rat kidney and bladder of the toad Bufo marinus

Harris

Jenner

1972

British J Pharmacology

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Summary1. The effect of intravenous infusions of various ions on the antidiuretic action of antidiuretic hormone has been studied in rats. 2. Lithium (13 mmol/l.) reversibly inhibits the antidiuretic responses. Similar concentrations of potassium, rubidium, strontium, magnesium, choline and calcium do not. Lithium has a similar effect on the antidiuretic activity of oxytocin.3. The inhibition is not simply related to blood nor whole body lithium concentrations. 4. Lithium (2 mmol/l.) in contact with the serosal surface also inhibits the transport of water facilitated by either 0 5 u/i. antidiuretic hormone or 1 1 mmol/l. cyclic adenosine monophosphate in the isolated toad bladder. 5. Choline (2 mmol/l.) on the serosal surface also inhibits the transport of water facilitated by vasopressin in the toad bladder.

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“…Listed among the less commonly occurring side effects of the administration of lithium salts are polyuria and polydipsia (1). Recently, both clinical observations (2,3) and preliminary data obtained in experimental animals (4,5) suggest that lithium can produce a reversible nephrogenic diabetes insipidus syndrome. However, the precise pathophysiology of the renal defect remains undefined.…”

Section: Introductionmentioning

confidence: 99%

Lithium-induced nephrogenic diabetes insipidus: in vivo and in vitro studies

Singer¹,

Rotenberg²,

Puschett³

1972

J. Clin. Invest.

178

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A B S T R A C T The physiological basis for the polyuria and polydipsia occurring in some manic-depressive patients treated with lithium salts was studied in vivo and in vitro. Three lithium-treated polyuric patients, in whom other causes of a concentrating defect were excluded, had abnormal urinary concentrating abilities after a standard water depreviation test. Two of these patients failed to respond to exogenous vasopressin (ADH) and one had a subnormal response. The abilities of these patients to excrete solute-free water (CI20) was comparable to normal subjects during steady-state water diuresis, suggesting no gross abnormalities in sodium transport. However, each of these patients demonstrated abnormally low capacities to reabsorb solutefree water (TCHo) under hydropenic conditions after administration of hypertonic saline and vasopressin. These in vivo findings demonstrate at least a nephrogenic basis for the diabetes insipidus syndrome manifested by these three patients.The defect in water transport was further characterized in toad urinary bladders in vitro. Short-circuit current (I) and water flow (W) were studied under basal, ADH-stimulated, and cyclic adenosine 3',5'-monophosphate (c-AMP)-stimulated conditions. Increasing mucosal [Li']

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Lithium-induced diabetes insipidus-like syndrome

Cited by 109 publications

References 7 publications

Inhibition by lithium of the hydroosmotic action of vasopressin in the isolated perfused cortical collecting tubule of the rabbit.

Inhibition by lithium of the hydroosmotic action of vasopressin in the isolated perfused cortical collecting tubule of the rabbit.

Some aspects of the inhibition of the action of antidiuretic hormone by lithium ions in the rat kidney and bladder of the toad Bufo marinus

Lithium-induced nephrogenic diabetes insipidus: in vivo and in vitro studies

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